Effect of p38MAPK inhibition on receptor activator of nuclear factor-κB ligand and osteoprotegerin expressions in osteoblasts
- VernacularTitle:p38MAPK抑制对成骨细胞核因子-κB受体激活配体和骨保护素表达的影响
- Author:
Ruixia LI
;
Xirong XIAO
;
Chao GU
;
Yan XU
;
Bin LI
- Publication Type:Journal Article
- Keywords:
p38MAPK;
17β-estradiol;
raloxifene;
osteoblast;
osteoprotegerin;
receptor activator of nuclear factor-κB ligand
- From:
Fudan University Journal of Medical Sciences
2010;37(1):39-42
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of p38MAPK in the differentiation of murine osteoblasts, and to observe the expressions of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG). Methods The calvarial osteoblasts of newborn BALB/c mice were cultured in MEM medium containing 10% NCS. Raloxifene (10~(-7) mol/L) and 17β-estradiol (10~(-8) mol/L) were added respectively when cells reached 70%-80% confluence combined with or without 5 μmol/L SB202190, an inhibitor of p38MAPK. The osteoblasts alkaline phosphatase activity assays were performed 72 hours later using PNPP method, and mRNA levels of alkaliphosphatase (ALP), OPG and RANKL were determined by RT-PCR. Results 17β-estradiol and raloxifene increased ALP activity and ALP mRNA level in osteoblasts in vitro which were blocked by p38MAPK inhibitor.The mRNA levels of RANKL and OPG were up-regulated by 17β-estradiol and raloxifene while the ratio of OPG/RANKL kept constant. SB202190 (5 μmol/L) inhibited the highly expressed RANKL and OPG in osteoblasts, and obviously decreased the ratio of OPG/RANKL. Conclusions p38MAPK inhibition blocked the differentiation of osteoblasts and decreased the up-regulated OPG and RANKL expressions in osteoblasts significantly (P<0.05).
